Skin Fungal infections How to treat

What are the topical agents for  skin Fugal infections ???? Topical Agents

A 1 or 2 week course of group  VI to VII topical steroids  may be all that  is necessary   . long  term continuous use of  topical steroids in skin  fold areas may result in atrophy and striae   0.1%  tacrolimus  may  be used   as an anti inflammatory  agent instead of topical   steroids   for initial    treatment or for cases   requiring   long term intermittent    treatment  Ciclopirox cream  or lotion    twice daily  for 1-2 weeks  or until   resolved  is another option .  It  is a good practice  to add a  topical anti yeast  medication, such   as miconazole creams with   topical   steroids. To separate and expose   skin effectively  in order to promote  dryness  administer   while  the patient is in the supine   position. After clinical   resolution topical   antifungal   treatments may be  continued twice weekly to prevent recurrence   and topical  steroids should be stopped.

Gentian violet      0.25to 2.0 5  and Castellani paint    are older   remedies  which   are effective but may sting and will stain clothing  bed linen and skin  

Systemic Agents

Outside  the setting  of chronic  mucocutenous   candiadiasis   chronic  systemic  suppressive    therapy  in immune suppressed  individuals    is discouraged due to the risk of colonization  with   resistant organisms.

Fulconazole

50 to 100 mg  daily for 14 days

150 mg  weekly for 2- 4  weeks

Itraconazole 200 mg  twice  daily for 14 days .

Tinea corporis – Grisceofulvin -500-1000 mg  / ay   ( microsize )   or 375  - 500 mg /d  ( ultramicrosize )  x 2-4 weeks , Fluconazole – 150mg / week  2-4 weeks , terbinafine – 250 mg daily x 1-2 weeks , Itraconazole – 200mg / day x  1 week or 100 mg / day x2 weeks , Ketovonazole – 200-400  mg /day  for 2 weeks

Tinea  corporis (children ) Griseofulvin 15-20 mg /kg / day   ( microsize suspension )x2-4 weeks , Fluconazole -6 mg / kg/week  2-4 weeks , Terbinafine – 125 mg daily x 1weeks , Itraconazole – 3-5 mg / kg / day ( maximum 200  mg ) x 1 week ,Ketovonazole – not recommended

Tinea Pedis/manuum – Griseofulvin – 750-1000 mg  / day  ( microsize )  or  500- 750 mg / d ( ultramicrosize )  x 6-12 weeks ,  Fluconazole – 150-200 mg / week  x 4-6 weeks , Terbinafine – 250 mg daily x 2 weeks , Itraconazole   - 200-400 mg / day x 1 week , Ketoconazole – not recommended

 Tinea Pedis / manuum ( children )  Griseofulvin -  15-20  mg / kg / day  ( microsize  suspension ) x 4 weeks , Fluconazole   6 mg / kg / week x 4-6 weeks , Terbinafine -125  mg ( < 20-40 kg )  or 250 mg ( > 40 kg ) x 2 week , Itraconazole -  3-5 mg / kg /day ( maximum 200 mg ) x 1 week , Katoconazole – not  recommended  

Tinea    Versicolor -  Griseofulvin – Not recommended , Fluconazole – 400 mg single dose repeat in 2 weeks   in needed , Teribinafine – oral therapy not   effective ,Itraconazole -  200 mg / day x 1 week Prophylaxis 200 mg BD 1 day / month  for 6 months in recurrent   disease , Ketoconazole – 400 mg single dose   400 mg single 200 mg OD for 5 days , 400 mg once a month for recurrent  disease

Vaginal candidiasis –Grisofulvin- Not effective , Fluconazole  - 200-400  mg daily  for 5 days ,  Tribinfine – Not effective , Itraconazole – 200 mg 3-5 days , Katoconazole -  150 mg single  dose

Fungal Infection

 Classification of fungi

Zygomycetes

Basidiomycetes

Ascomycetes

Hyphomycetes

The  ability   of fungi  to cause   disease   appears to be   an accidental  phenomenon. With the exception of  a few  dermatophytes pathogenicity  among  the fungi  is not necessary for the  maintenance or dissemination of the species.

The  two major  physiological  barriers to fungal  growth  within the human   body are temperature and redox   potential  of non living   metabolizing  tissue  . In addition   the body  has a highly  efficient   set of cellular  defences  to combat fungal proliferation. Thus the    mechanism of fungal  pathogenicity  is its ability  to adapt to the tissue   environment and to withstand  the lytic   activity of  the host’s   cellular defenses.

In general the development of human  mycoses is related   primarily to the  immunological status    of the host   and environmental   exposure  rather than to the infecting organism. A small  number of fungi has the ability to cause infections  in  normal   healthy humans  by  having   a unique enzymatic capacity   , exhibiting   thermal   dimorphism and   by having     an ability to block   the cell mediated immune defenes of the host. There are  then many opportunistic fungi   which    cause infections almost exclusively in debilitated  patients whose normal   defence   mechanisms  are impaired. The organisms involved  are cosmopolitan   fungi which   have a very low inherent virulence. Currently   there has been   a dramatic increase in fungal   infections of this type  in particular  candiadiasis   cryptococcosis  aspergillosis   and  zygomyocsis. More   recently  described  mycoses  of this  category  include hyalohyphomycosis and phaeohyphomycosis.

Fungal infections of the skin can be classified  into three main   types

Superficial fungal  infections

Caused  by fungi   that are  capable of colonizing   and superficially invading  skin and mucosal   sites

1.  Candida  species

2.  Malassezia  species

3.  Dermatophytes

4.  Peidra

5.  Tinea nigra

6.  The  subcutaneous  mycoses

Occur  after percutaneous  inoculation

i.                  Mycentoma

ii.               Chromoblastomycosis

iii.            Sporotrichosis

iv.            Zygomycosis

1.  Entomophthoramycosis

2.  Mucormycosis

3.  Hyalohyphomycosis

4.  Phaeohyphomycosis

Systemic fungal infections with  cutaneous  dissemination

Occur  most often  with host defense  defects Primary    lung infection disseminates  hematogenously to multiple   organ systems  including the skin aspergillosis   mucormycosis  cryptococcosis Histoplasmosis   North American  blastomycosis  coccidiodomyocosis  and peniciliosis.